Your example of polar bear is extreme example. There are millions of people ,relatives/brothers living under one roof ,eating same thing,living in same town country ,eating same doing same. Some starts to go bald or bald while others don't.why does the same or not so different environment and behavior have varied impact on people.
I would like to share my thoughts here both from reading and also personal experience.
First of all, the galea theory is wrong. I have friends who are complete junkies, friends who have heads the size of an alien and they are Norwood zero. Not only that, many of them grow very long hair.
The scalp expanding theory is again wrong for the same reasons. You don’t need studies and idiotic speculations to stir water with no purpose.
The scalp weight theory is also wrong. Head over to old rave parties videos, where people have grotesque posture and choke on mdmas yet maintain a perfect hairline.
The DHT theory is a big one. It is split into many sub theories. I can tell you that I have friends who have taken every anabolic steroid on the market and their hairline is the same. Tons and tons of examples can be found in the fitness world. The same goes for diet, the same goes for sex life etc. To put it in simple terms, there are two categories: those who bald and those who don’t bald. Those who bald try every environmental change in the book and still bald. Those who don’t bald try every sin in the book and still don’t bald. There is also a third category, the people who are not balding but think they are. Those are the reason for misinformation and confusion and this forum has plenty. Those are the ones crying about hair all the time, they try every drug possible and have delusions of maintenance or drug inefficacy.
I am a Norwood 5 at the age of 29. I have lost hair since 16, my hair texture, thickness and strength changed through my teenage years when hormones spiked. I also have hypothyroidism.
I took Finasteride and dutasteride last year. I am a perfect candidate because I am fucked good from his condition and I can testify if the drug works or not. The drug worked wonders. Hair all over the front, tiny resting hairs constantly falling out and being replaced by new strong darker ones. However, it gave me tits. So I discontinued it. I would be a Norwood 2-3 by the end of a single year no doubt.
What do we make of this? That the drug works as intended to people with an actual problem. We also conclude that whatever it may be, dht, tension or another mechanism, it is held partially responsible for the classic androgenic alopecia. People have to realize diet is useless at reversing it. My diet is impeccable and I don’t smoke or drink, I don’t even drink coffee. So yes, the drug works and dht does play a role.
However, it is important to mention that my testosterone levels were small to begin with. Both my LH and FSH are just above the baseline and my total T levels are below medium, however both my shbg and free T levels are GOOD, which means I’m not suffering from anything. My DHT levels were literally in the mid levels. Just keep this in mind.
The consequences from the drug were there. Fat tissue, growing fatty nipples with no lump, relaxation in the muscles, loss of libido and a general feminization. Which only comes to show that the drug works. For the people who keep saying it’s an estrogen value game, don’t. My e2 levels were always on 34, two months later on the drug they were on 27, which is an excellent value. I still grew tits from day 1 though. For the record everything is now reversed upon discontinuation.
The drug also drops your natural progesterone to zero, since it is a synthetic form. Apparently it is what may cause the gyno although it’s more of an androgen issue, the drug pretty much takes you back to your early teens. More on that on a future topic, I promise.
It’s worth mentioning I had regrowth everywhere on my shinny parts of scalp which shows that calcification for a decade doesn’t kill the follicles. I am a believer of that.
So to conclude I think antiandrogens are useless not because they don’t work - they do work to those with an actual problem - but because they alter one’s hormonal profile in scary ways and also permanent ways because the point is to take the drug forever like thyroxine for example.
I want to mention now a term that is very vague, very scary and very powerful. And that term is “stress”. Now stress is chaotic it has many forms and is understood differently by people.
But there is one type of stress that I have seen in every single person I met that has alopecia. That is the sudden, traumatic event stress. Even in movies have you noticed that people who go through such an event early in their lives are shown later in horrible condition AND bald? It’s almost in every movie. Or maybe they want to portray baldness as a bad thing, who knows. The point is that I’ve known lads who lost all their hair suddenly in their mid thirties, from ponytail to nw6 after a loss of a loved one. Classic horeshoe pattern and everything. How do you explain that, since alopecia is supposed to happen earlier? Follicles decided to be sensitive after the loss of the loved one? And if so, WHY and HOW?
It is therefore my belief that two cases can be true: sudden traumatic stress turns on the follicular sensitivity and alopecia OR follicular sensitivity is there and you lose hair from early teen as usual. You can see though that one theory contradicts the other yet both of them happen! How?!
The answer may be the word “inflammation”. So either the follicular predisposition is utter bullshit and alopecia is a 100% inflammation game OR follicular sensitivity to DHT exists since birth but inflammation ALONE is the key to turn it on. That would explain why someone loses hair from 16 and someone else from 45. And inflammation increases with age and health problems which is why many lose hair after their 60s, no? So maybe Finasteride doesn’t really work by blocking DHT but blocks or stops temporarily the INFLAMMATION PROCESS. Now what would that inflammation be?
Take for example the male to female people. Excellent examples of success. What do they block? They block testsosterone, my friends. Not dht, not estrogen, not some other pathway bullshit. They block T and when they block it completely, guess what: full heads of hair. Before someone says: “uff idiot that’s because blocking t blocks dht hello?” I will say this: put an hrt case next to a case of 10mg of avodart ed you will find that the zero T case isn’t even a match, it has won by a landslide against the avodart case. Almost Zero DHT on both, but one case with almost zero T
The problem of alopecia lies with testosterone. Testosterone genetic code, maybe infected testosterone cells? Who knows... but that is where you need to focus! And the people who feel great libido on Finasteride it isn’t because of total T levels. In my opinion it is androgenic sensitivity, number of T versus DHT receptors or maybe some other mechanism but it has nothing to do with T unless you get a blood test that measures total T / SHBG = free T.
The problem lies with testosterone 100% and one of its mechanisms or byproducts that we have yet to discover.